Pub Date : 2025-08-25DOI: 10.1016/j.metop.2025.100387
Abdullah Al Lawati , Ayman N. Alhabsi , Ali Al Sabti , Raksha S. Krishnan , Sulaiman Alkindi , Srijit Das , Mohammed Al-Abri
Dumping syndrome (DS) is a known complication following bariatric surgery, caused by rapid gastric emptying into the small intestine. It presents in two forms: early dumping, with gastrointestinal and vasomotor symptoms occurring within 30–60 min after meals; and late dumping, which arises 1–3 h postprandially due to reactive hypoglycaemia. Standard management includes dietary changes and medications, but tolerability and long-term efficacy are variable. Recently, interest has grown in using natural products and nutritional compounds as adjuncts or alternatives. Fibre-rich foods, sugar substitutes, and medicinal plants may delay gastric emptying, reduce glucose spikes, or modulate gut hormones such as GLP-1 and GIP. Several phytochemicals, polyphenols, flavonoids, alkaloids, and terpenoids have demonstrated promise in reducing DS symptoms, especially in late dumping. Functional foods may enhance satiety, slow carbohydrate absorption, and improve glycaemic control. Although most data are from preclinical or limited clinical studies, natural compounds appear to be well-tolerated and safe, offering potential advantages over standard pharmacological agents. This review summarises emerging evidence on the role of natural products in managing DS, their mechanisms of action, and their clinical relevance in post-bariatric care. The findings aim to support translational metabolic care and provide practical guidance for clinicians and dietitians managing DS in diverse patient populations.
{"title":"Supplementary use of natural products in managing dumping syndrome: Exploring dietary and phytochemical interventions","authors":"Abdullah Al Lawati , Ayman N. Alhabsi , Ali Al Sabti , Raksha S. Krishnan , Sulaiman Alkindi , Srijit Das , Mohammed Al-Abri","doi":"10.1016/j.metop.2025.100387","DOIUrl":"10.1016/j.metop.2025.100387","url":null,"abstract":"<div><div>Dumping syndrome (DS) is a known complication following bariatric surgery, caused by rapid gastric emptying into the small intestine. It presents in two forms: early dumping, with gastrointestinal and vasomotor symptoms occurring within 30–60 min after meals; and late dumping, which arises 1–3 h postprandially due to reactive hypoglycaemia. Standard management includes dietary changes and medications, but tolerability and long-term efficacy are variable. Recently, interest has grown in using natural products and nutritional compounds as adjuncts or alternatives. Fibre-rich foods, sugar substitutes, and medicinal plants may delay gastric emptying, reduce glucose spikes, or modulate gut hormones such as GLP-1 and GIP. Several phytochemicals, polyphenols, flavonoids, alkaloids, and terpenoids have demonstrated promise in reducing DS symptoms, especially in late dumping. Functional foods may enhance satiety, slow carbohydrate absorption, and improve glycaemic control. Although most data are from preclinical or limited clinical studies, natural compounds appear to be well-tolerated and safe, offering potential advantages over standard pharmacological agents. This review summarises emerging evidence on the role of natural products in managing DS, their mechanisms of action, and their clinical relevance in post-bariatric care. The findings aim to support translational metabolic care and provide practical guidance for clinicians and dietitians managing DS in diverse patient populations.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100387"},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144902322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-24DOI: 10.1016/j.metop.2025.100388
Qiong Huang , Xiuben Du , Wenwei Ouyang , Jing Wang , Xusheng Liu
Background
Sarcopenic obesity (SO) combines reduced muscle mass and increased fat, elevating health risks in older adults. The triglyceride-glucose (TyG) index, a marker of insulin resistance, is associated with metabolic dysfunction. However, its role in predicting mortality in SO remains unclear. This study investigates the TyG index as a potential predictor of all-cause mortality in older adults with SO.
Methods
This study examined SO trends using data from 30,137 adults with dual-energy X-ray absorptiometry (DXA) and body fat measurements (1999–2018). For mortality analysis, 706 participants from NHANES 1999–2004 were included. Sarcopenia was defined according to the 2014 FNIH criteria. Statistical analyses, including Cox regression, cubic splines, and subgroup analyses, were employed to investigate the association between the TyG index and all-cause mortality in SO, as well as mortality variations among NHANES participants.
Results
Older age groups exhibit higher SO prevalence rates, with a notable upward trend in the >70 years group, while younger groups maintain lower rates. Trend analysis indicates no significant change from 1999 to 2006 but suggests a moderate, near-significant increase from 2011 to 2018. There was a U-shaped association between the TyG index and all-cause mortality. After full adjustment, adults in TyG group 1 (less than 3.25) had a 78.1 % higher risk (hazard ratio, 1.781; 95 % CI, 1.406–2.256; p < 0.001), and those in TyG group 5 (6.66 or greater) had a 74.5 % higher risk (hazard ratio, 1.745; 95 % CI, 1.211–2.516; p = 0.003) compared to the reference group (TyG group 3, 4.25 to 5.25). Subgroup analysis by age revealed that, among participants aged 70 and older, the group with the lowest mortality risk transitioned from Group 3 to Group 2. Furthermore, the analysis of varying mortality reveals that Group 5 (HR: 3.088; 95 % CI: 1.462–6.520; p = 0.003) is significantly associated with an increased risk of cardiovascular disease (CVD) mortality compared to Group 3. Similarly, TyG Group 1 demonstrates a significantly higher risk of mortality from other causes (HR: 2.253; 95 % CI: 1.207–4.206; p = 0.011) relative to Group 3. No significant associations are observed for malignant neoplasms, respiratory diseases, or cerebrovascular/Alzheimer's diseases.
Conclusion
This national cohort study identified a U-shaped association between the TyG index and all-cause mortality among SO patients, with increased risks observed at both low and high TyG levels. Age-specific analyses further reveal variations in this relationship, underscoring the importance of tailored strategies to enhance metabolic health and reduce mortality risks.
背景：肌少性肥胖（SO）结合了肌肉量减少和脂肪增加，增加了老年人的健康风险。甘油三酯-葡萄糖（TyG）指数是胰岛素抵抗的标志，与代谢功能障碍有关。然而，它在预测SO死亡率中的作用仍不清楚。本研究探讨了TyG指数作为老年SO患者全因死亡率的潜在预测因子。方法：本研究使用1999-2018年30137名成年人的双能x射线吸收仪（DXA）和体脂测量数据来研究SO趋势。死亡率分析纳入1999-2004年NHANES的706名参与者。骨骼肌减少症根据2014年FNIH标准定义。统计分析，包括Cox回归、三次样条和亚组分析，用于调查TyG指数与SO全因死亡率之间的关系，以及NHANES参与者之间的死亡率变化。结果各年龄组SO患病率较高，70岁年龄组患病率上升趋势明显，较年轻年龄组患病率较低。趋势分析表明，从1999年到2006年没有显著变化，但从2011年到2018年略有增加。TyG指数与全因死亡率呈u型相关。完全调整后，TyG组1（小于3.25）的成年人与参照组（TyG组3,4.25 ~ 5.25）相比，风险高78.1%（风险比1.781;95% CI, 1.406 ~ 2.256; p < 0.001）， TyG组5（6.66或更高）的成年人风险高74.5%（风险比1.745;95% CI, 1.211 ~ 2.516; p = 0.003）。按年龄进行的亚组分析显示，在70岁及以上的参与者中，死亡风险最低的一组从第3组过渡到第2组。此外，对不同死亡率的分析显示，与第3组相比，第5组（HR: 3.088; 95% CI: 1.462-6.520; p = 0.003）与心血管疾病（CVD）死亡率风险增加显著相关。同样，TyG组1的其他原因死亡风险明显高于组3 （HR: 2.253; 95% CI: 1.207-4.206; p = 0.011）。恶性肿瘤、呼吸系统疾病或脑血管/阿尔茨海默病未观察到显著相关性。这项全国性队列研究发现，在SO患者中，TyG指数与全因死亡率之间存在u型相关性，TyG水平高低均会增加风险。特定年龄的分析进一步揭示了这种关系的变化，强调了定制策略的重要性，以增强代谢健康和降低死亡风险。
{"title":"Relationship between triglyceride-glucose index and all-cause mortality in older adults with sarcopenic obesity","authors":"Qiong Huang , Xiuben Du , Wenwei Ouyang , Jing Wang , Xusheng Liu","doi":"10.1016/j.metop.2025.100388","DOIUrl":"10.1016/j.metop.2025.100388","url":null,"abstract":"<div><h3>Background</h3><div>Sarcopenic obesity (SO) combines reduced muscle mass and increased fat, elevating health risks in older adults. The triglyceride-glucose (TyG) index, a marker of insulin resistance, is associated with metabolic dysfunction. However, its role in predicting mortality in SO remains unclear. This study investigates the TyG index as a potential predictor of all-cause mortality in older adults with SO.</div></div><div><h3>Methods</h3><div>This study examined SO trends using data from 30,137 adults with dual-energy X-ray absorptiometry (DXA) and body fat measurements (1999–2018). For mortality analysis, 706 participants from NHANES 1999–2004 were included. Sarcopenia was defined according to the 2014 FNIH criteria. Statistical analyses, including Cox regression, cubic splines, and subgroup analyses, were employed to investigate the association between the TyG index and all-cause mortality in SO, as well as mortality variations among NHANES participants.</div></div><div><h3>Results</h3><div>Older age groups exhibit higher SO prevalence rates, with a notable upward trend in the >70 years group, while younger groups maintain lower rates. Trend analysis indicates no significant change from 1999 to 2006 but suggests a moderate, near-significant increase from 2011 to 2018. There was a U-shaped association between the TyG index and all-cause mortality. After full adjustment, adults in TyG group 1 (less than 3.25) had a 78.1 % higher risk (hazard ratio, 1.781; 95 % CI, 1.406–2.256; p < 0.001), and those in TyG group 5 (6.66 or greater) had a 74.5 % higher risk (hazard ratio, 1.745; 95 % CI, 1.211–2.516; p = 0.003) compared to the reference group (TyG group 3, 4.25 to 5.25). Subgroup analysis by age revealed that, among participants aged 70 and older, the group with the lowest mortality risk transitioned from Group 3 to Group 2. Furthermore, the analysis of varying mortality reveals that Group 5 (HR: 3.088; 95 % CI: 1.462–6.520; p = 0.003) is significantly associated with an increased risk of cardiovascular disease (CVD) mortality compared to Group 3. Similarly, TyG Group 1 demonstrates a significantly higher risk of mortality from other causes (HR: 2.253; 95 % CI: 1.207–4.206; p = 0.011) relative to Group 3. No significant associations are observed for malignant neoplasms, respiratory diseases, or cerebrovascular/Alzheimer's diseases.</div></div><div><h3>Conclusion</h3><div>This national cohort study identified a U-shaped association between the TyG index and all-cause mortality among SO patients, with increased risks observed at both low and high TyG levels. Age-specific analyses further reveal variations in this relationship, underscoring the importance of tailored strategies to enhance metabolic health and reduce mortality risks.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100388"},"PeriodicalIF":2.7,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Helicobacter pylori (H. pylori) infection is a globally prevalent gastrointestinal pathogen increasingly linked to various extra-gastric non-communicable diseases (NCDs). This review addresses the guiding question: What epidemiological and mechanistic links explain the association between H. pylori infection and chronic conditions such as cardiovascular disease (CVD), metabolic dysfunction-associated steatotic liver disease (MASLD), and type 2 diabetes mellitus (T2DM)?
The manuscript synthesizes evidence from epidemiological studies and mechanistic research. In CVD, H. pylori exacerbates chronic vascular inflammation, endothelial dysfunction, and autoimmune-like responses such as molecular mimicry. In MASLD, H. pylori induces insulin resistance (IR), hepatic inflammation, and microbiota-mediated liver injury, although findings remain inconclusive across populations. For T2DM, multiple pathways including NLRP3 inflammasome activation, hormonal imbalances (e.g., ghrelin, leptin), and immune-genetic interactions involving TLR4 and SOCS3 suggest a role for H. pylori in metabolic dysregulation and impaired glycemic control. While researchers have not yet fully elucidated causality, these findings indicate H. pylori as a potential modifiable risk factor for NCDs. Future longitudinal and interventional studies are warranted to determine whether eradication of H. pylori can mitigate chronic disease.
{"title":"Helicobacter pylori infection and association with chronic diseases: A focus on cardiovascular disease, MASLD, and type 2 diabetes","authors":"Navid Maleki , Alireza Mohammadzadeh , Jalal Mardaneh , Hossein Pazoki , Elyas Nattagh-Eshtivani","doi":"10.1016/j.metop.2025.100385","DOIUrl":"10.1016/j.metop.2025.100385","url":null,"abstract":"<div><div><em>Helicobacter pylori</em> (<em>H. pylori</em>) infection is a globally prevalent gastrointestinal pathogen increasingly linked to various extra-gastric non-communicable diseases (NCDs). This review addresses the guiding question: What epidemiological and mechanistic links explain the association between H. pylori infection and chronic conditions such as cardiovascular disease (CVD), metabolic dysfunction-associated steatotic liver disease (MASLD), and type 2 diabetes mellitus (T2DM)?</div><div>The manuscript synthesizes evidence from epidemiological studies and mechanistic research. In CVD, <em>H. pylori</em> exacerbates chronic vascular inflammation, endothelial dysfunction, and autoimmune-like responses such as molecular mimicry. In MASLD, <em>H. pylori</em> induces insulin resistance (IR), hepatic inflammation, and microbiota-mediated liver injury, although findings remain inconclusive across populations. For T2DM, multiple pathways including NLRP3 inflammasome activation, hormonal imbalances (e.g., ghrelin, leptin), and immune-genetic interactions involving TLR4 and SOCS3 suggest a role for <em>H. pylori</em> in metabolic dysregulation and impaired glycemic control. While researchers have not yet fully elucidated causality, these findings indicate <em>H. pylori</em> as a potential modifiable risk factor for NCDs. Future longitudinal and interventional studies are warranted to determine whether eradication of <em>H. pylori</em> can mitigate chronic disease.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100385"},"PeriodicalIF":2.7,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-08DOI: 10.1016/j.metop.2025.100384
Sharvari S. Pandit , Prabhu Meganathan , Hemamalini Vedagiri
The gut microbiota, comprising trillions of microorganisms inhabiting the gastrointestinal tract, is essential to human health and disease. Recent research has illuminated the interactions between many components of human physiology and the gut microbiota, including immune function, metabolism, and neurological health. Central to maintaining this symbiotic relationship is the concept of dysbiosis – an imbalance in the makeup and roles of the gut microbiota. Dysbiosis of the gut microbiota has emerged as a significant factor in the pathogenesis of numerous health conditions, spanning from gastrointestinal disorders like inflammatory bowel disease and irritable bowel syndrome to systemic diseases such as obesity, metabolic syndrome, and even neurological disorders like depression and anxiety. While dysbiosis can result from a myriad of factors including antibiotic use, stress, and genetic predispositions, emerging evidence suggests that diet and lifestyle choices exert profound influences regarding the make-up and capabilities of the gut microbiota. In this review, We explore the complex interactions among lifestyle, nutrition, and gut microbial dysbiosis. In particular, we investigate how the gut microbiota can be modified and dysbiosis can be mitigated by dietary patterns, food composition, prebiotics, probiotics, and lifestyle factors including exercise, stress reduction, and good sleep hygiene. Restoring microbial balance and enhancing general health and well-being can be achieved through preventive and therapeutic measures that can be made more effective by understanding how dietary and lifestyle changes might affect the gut microbiota. Through this exploration, we aim to elucidate the possibility of using lifestyle and dietary modifications as tools for managing gut microbial dysbiosis.
{"title":"Harmonizing gut microbiota dysbiosis: Unveiling the influence of diet and lifestyle interventions","authors":"Sharvari S. Pandit , Prabhu Meganathan , Hemamalini Vedagiri","doi":"10.1016/j.metop.2025.100384","DOIUrl":"10.1016/j.metop.2025.100384","url":null,"abstract":"<div><div>The gut microbiota, comprising trillions of microorganisms inhabiting the gastrointestinal tract, is essential to human health and disease. Recent research has illuminated the interactions between many components of human physiology and the gut microbiota, including immune function, metabolism, and neurological health. Central to maintaining this symbiotic relationship is the concept of dysbiosis – an imbalance in the makeup and roles of the gut microbiota. Dysbiosis of the gut microbiota has emerged as a significant factor in the pathogenesis of numerous health conditions, spanning from gastrointestinal disorders like inflammatory bowel disease and irritable bowel syndrome to systemic diseases such as obesity, metabolic syndrome, and even neurological disorders like depression and anxiety. While dysbiosis can result from a myriad of factors including antibiotic use, stress, and genetic predispositions, emerging evidence suggests that diet and lifestyle choices exert profound influences regarding the make-up and capabilities of the gut microbiota. In this review, We explore the complex interactions among lifestyle, nutrition, and gut microbial dysbiosis. In particular, we investigate how the gut microbiota can be modified and dysbiosis can be mitigated by dietary patterns, food composition, prebiotics, probiotics, and lifestyle factors including exercise, stress reduction, and good sleep hygiene. Restoring microbial balance and enhancing general health and well-being can be achieved through preventive and therapeutic measures that can be made more effective by understanding how dietary and lifestyle changes might affect the gut microbiota. Through this exploration, we aim to elucidate the possibility of using lifestyle and dietary modifications as tools for managing gut microbial dysbiosis.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100384"},"PeriodicalIF":2.7,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-29DOI: 10.1016/j.metop.2025.100382
Salya F. Alfadli , Yazeed S. Alotaibi , Maha J. Aqdi , Latifah A. Almozan , Zahra B. Alzubaidi , Hammad A. Altemani , Shaden D. Almutairi , Hussain A. Alabdullah , Alaa Ahmed Almehmadi , Abdulrahman L. Alanzi , Ahmed Y. Azzam
Introduction
Continuous glucose monitoring (CGM) technologies have been advancing rapidly, but evidence on their comparative effectiveness stills limited to date yet. We conducted a systematic review and meta-analysis to evaluate and investigate the impact of CGM systems on glycemic control in adults with type 1 diabetes.
Methods
We searched electronic literature databases from inception through April 30, 2025, for comparative studies investigating CGM systems with standard monitoring or different CGM technologies in adults with type 1 diabetes. Primary outcomes included HbA1c reduction, time in range (TIR), and hypoglycemia reduction. We performed random-effects meta-analyses, network meta-analysis, and subgroup analyses by baseline HbA1c and intervention duration. Evidence quality was assessed using GRADE methodology.
Results
Twenty-seven studies with total of 2975 participants were included. CGM significantly reduced HbA1c compared to standard monitoring (mean difference: 0.38 %, 95 % CI: 0.49 to −0.27 %). TIR increased by 7.9 % (95 % CI: 5.8–10.0 %), representing 114 additional minutes daily in best range. Real-time CGM showed advantages over intermittently scanned CGM for TIR (+5.63 %, P-value<0.001) and hypoglycemia reduction (−1.28 %, P-value<0.001). Automated closed-loop systems achieved the highest ranking in network meta-analysis (SUCRA = 0.92). Benefits were greater among patients with higher baseline HbA1c (>8.5 %: 0.68 % reduction in HbA1c vs. <7.5 %: 0.24 % reduction in HbA1c, P-value = 0.009).
Conclusions
CGM technologies significantly improve glycemic control in adults with type 1 diabetes, with greater benefits for those with higher baseline HbA1c. Advanced systems demonstrate progressively greater improvements, with automated closed-loop systems showing the strongest evidence of effectiveness. These findings support broader implementation of CGM technologies, with selection tailored to individual patient needs.
{"title":"Effectiveness of continuous glucose monitoring systems on glycemic control in adults with type 1 diabetes: A systematic review and meta-analysis","authors":"Salya F. Alfadli , Yazeed S. Alotaibi , Maha J. Aqdi , Latifah A. Almozan , Zahra B. Alzubaidi , Hammad A. Altemani , Shaden D. Almutairi , Hussain A. Alabdullah , Alaa Ahmed Almehmadi , Abdulrahman L. Alanzi , Ahmed Y. Azzam","doi":"10.1016/j.metop.2025.100382","DOIUrl":"10.1016/j.metop.2025.100382","url":null,"abstract":"<div><h3>Introduction</h3><div>Continuous glucose monitoring (CGM) technologies have been advancing rapidly, but evidence on their comparative effectiveness stills limited to date yet. We conducted a systematic review and meta-analysis to evaluate and investigate the impact of CGM systems on glycemic control in adults with type 1 diabetes.</div></div><div><h3>Methods</h3><div>We searched electronic literature databases from inception through April 30, 2025, for comparative studies investigating CGM systems with standard monitoring or different CGM technologies in adults with type 1 diabetes. Primary outcomes included HbA1c reduction, time in range (TIR), and hypoglycemia reduction. We performed random-effects meta-analyses, network meta-analysis, and subgroup analyses by baseline HbA1c and intervention duration. Evidence quality was assessed using GRADE methodology.</div></div><div><h3>Results</h3><div>Twenty-seven studies with total of 2975 participants were included. CGM significantly reduced HbA1c compared to standard monitoring (mean difference: 0.38 %, 95 % CI: 0.49 to −0.27 %). TIR increased by 7.9 % (95 % CI: 5.8–10.0 %), representing 114 additional minutes daily in best range. Real-time CGM showed advantages over intermittently scanned CGM for TIR (+5.63 %, P-value<0.001) and hypoglycemia reduction (−1.28 %, P-value<0.001). Automated closed-loop systems achieved the highest ranking in network meta-analysis (SUCRA = 0.92). Benefits were greater among patients with higher baseline HbA1c (>8.5 %: 0.68 % reduction in HbA1c vs. <7.5 %: 0.24 % reduction in HbA1c, P-value = 0.009).</div></div><div><h3>Conclusions</h3><div>CGM technologies significantly improve glycemic control in adults with type 1 diabetes, with greater benefits for those with higher baseline HbA1c. Advanced systems demonstrate progressively greater improvements, with automated closed-loop systems showing the strongest evidence of effectiveness. These findings support broader implementation of CGM technologies, with selection tailored to individual patient needs.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100382"},"PeriodicalIF":2.7,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-24DOI: 10.1016/j.metop.2025.100380
Shuwei Tian , Xiaoli Zhang , Jiayong Yu , Juan Cai , Danni Wei , Siqi Li , Pengfei Cai , Wei Song , Suihan Feng , Mengle Shao , Haizhou Li
Adipose tissue, a pivotal metabolic regulator, houses diverse stromal cell populations influencing its dynamic functions. Recent omics studies, including transcriptomics and proteomics, have revealed intricate cellular heterogeneity, yet comprehensive metabolic profiling remains limited. Leveraging fluorescence-activated cell sorting (FACS), we isolated PDGFRα+ DPP4+ and PDGFRα+ DPP4- adipose stromal cells (ASCs) from human orbital adipose tissue (OAT). Integrating gene expression analysis, in vitro adipogenesis assays, and quantitative lipidomics, we characterized their functional and metabolic distinctions. DPP4- ASCs exhibited enhanced adipogenic potential and distinct lipidomic profiles, featuring elevated ceramides and triacylglycerols compared to DPP4+ ASCs. Differential gene expression highlighted metabolic and adipogenic gene signatures reflective of their functional roles in adipose tissue remodeling. Our findings underscore the metabolic heterogeneity within OAT stromal fibroblasts, implicating DPP4- ASCs as potent regulators of adipogenesis and metabolic homeostasis. These insights enhance our understanding of adipose tissue plasticity and may inform therapeutic strategies for conditions like thyroid-associated ophthalmopathy.
{"title":"Quantitative lipidomic analysis reveals distinct metabolic traits between stromal cell subpopulations in human orbital adipose tissue","authors":"Shuwei Tian , Xiaoli Zhang , Jiayong Yu , Juan Cai , Danni Wei , Siqi Li , Pengfei Cai , Wei Song , Suihan Feng , Mengle Shao , Haizhou Li","doi":"10.1016/j.metop.2025.100380","DOIUrl":"10.1016/j.metop.2025.100380","url":null,"abstract":"<div><div>Adipose tissue, a pivotal metabolic regulator, houses diverse stromal cell populations influencing its dynamic functions. Recent omics studies, including transcriptomics and proteomics, have revealed intricate cellular heterogeneity, yet comprehensive metabolic profiling remains limited. Leveraging fluorescence-activated cell sorting (FACS), we isolated PDGFRα+ DPP4+ and PDGFRα+ DPP4- adipose stromal cells (ASCs) from human orbital adipose tissue (OAT). Integrating gene expression analysis, in vitro adipogenesis assays, and quantitative lipidomics, we characterized their functional and metabolic distinctions. DPP4- ASCs exhibited enhanced adipogenic potential and distinct lipidomic profiles, featuring elevated ceramides and triacylglycerols compared to DPP4+ ASCs. Differential gene expression highlighted metabolic and adipogenic gene signatures reflective of their functional roles in adipose tissue remodeling. Our findings underscore the metabolic heterogeneity within OAT stromal fibroblasts, implicating DPP4- ASCs as potent regulators of adipogenesis and metabolic homeostasis. These insights enhance our understanding of adipose tissue plasticity and may inform therapeutic strategies for conditions like thyroid-associated ophthalmopathy.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100380"},"PeriodicalIF":0.0,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144714460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-22DOI: 10.1016/j.metop.2025.100381
Ebrahim Abbasi, Iraj Khodadadi
High-fat diet (HFD) poses various health risks, such as obesity, insulin resistance (IR), fatty liver, gut microbiota dysbiosis, cognitive impairment, inflammation, and oxidative stress. HFD can alter gastrointestinal function and structure, resulting in changes of the intestinal mucosa, gastric secretions, intestinal connective tissue, intestinal motility, intestinal metabolomics profiles, and intestinal microbiota. The intestine and its microbiota process nutrients and produce molecules that can regulate insulin action and secretion. Changes in the gut microbiome (dysbiosis) and their products may have long-term effects that are not fully understood. Gut microbiota have long been documented to induce metabolic endotoxemia by releasing lipopolysaccharide, which causes systemic inflammation and insulin resistance (IR). HFD may has direct roles in the development of insulin resistance (IR). HFD can induce dysbiosis by reducing SCFAs and decreasing the activation of free fatty acid receptors (FFARs). Furthermore, HFD can increase the activation of the toll-like receptor (TLR) pathway. Hence, HFD by inducing inflammation, oxidative stress, endotoxemia, and hyperglycemia can increase the risk of IR. Therefore, this review aims to delineate the role of gut microbiota directly or indirectly involved in HFD-induced IR. These findings may clarify valuable preventive and therapeutic targets for countermeasures to IR in people who use the Western diet.
{"title":"High-fat diet may increase the risk of insulin resistance by inducing dysbiosis","authors":"Ebrahim Abbasi, Iraj Khodadadi","doi":"10.1016/j.metop.2025.100381","DOIUrl":"10.1016/j.metop.2025.100381","url":null,"abstract":"<div><div>High-fat diet (HFD) poses various health risks, such as obesity, insulin resistance (IR), fatty liver, gut microbiota dysbiosis, cognitive impairment, inflammation, and oxidative stress. HFD can alter gastrointestinal function and structure, resulting in changes of the intestinal mucosa, gastric secretions, intestinal connective tissue, intestinal motility, intestinal metabolomics profiles, and intestinal microbiota. The intestine and its microbiota process nutrients and produce molecules that can regulate insulin action and secretion. Changes in the gut microbiome (dysbiosis) and their products may have long-term effects that are not fully understood. Gut microbiota have long been documented to induce metabolic endotoxemia by releasing lipopolysaccharide, which causes systemic inflammation and insulin resistance (IR). HFD may has direct roles in the development of insulin resistance (IR). HFD can induce dysbiosis by reducing SCFAs and decreasing the activation of free fatty acid receptors (FFARs). Furthermore, HFD can increase the activation of the toll-like receptor (TLR) pathway. Hence, HFD by inducing inflammation, oxidative stress, endotoxemia, and hyperglycemia can increase the risk of IR. Therefore, this review aims to delineate the role of gut microbiota directly or indirectly involved in HFD-induced IR. These findings may clarify valuable preventive and therapeutic targets for countermeasures to IR in people who use the Western diet.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100381"},"PeriodicalIF":0.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144696747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.metop.2025.100378
Monica Peter , Mithra Balaji , Joe Varghese , Sam Marconi , Yesudhas Sudhakar , Felix Jebasingh , Padmanaban Venkatesan
Introduction
Diabetes in South Asians is driven primarily by impaired beta-cell function. When challenged with a high-calorie diet, this can result in metabolically unfavourable fat accumulation, which in turn worsens beta-cell function, thus constituting a vicious cycle. The investigators hypothesized that short-term mild-to-moderate weight loss induced by calorie restriction could break the cycle, resulting in significant improvements in beta-cell function. The objective of this study, therefore, was to evaluate the efficacy of a short-term weight loss program on body composition and beta-cell function.
Methods
As part of this quasi-experimental pre-post intervention study, 23 overweight normoglycemic participants underwent a low-calorie dietary intervention (∼1500 kcal/day) for a period of 4 weeks. Beta-cell function and insulin sensitivity were measured with a mixed meal challenge test (oral minimal model of glucose) before and after the intervention period. Changes in anthropometric parameters and body composition were also measured. The study was registered prospectively with the Clinical Trials Registry of India - CTRI/2023/04/051807 (https://ctri.nic.in/)
Results
Among the 23 participants in the study, 21 adhered to the intervention. The average weight loss was 3.5 % with an 11 % reduction in trunk fat mass. Beta-cell function, as measured by disposition index, increased by 128 % on average. Robust linear regression analysis showed that beta-cell function improved by 23 % for 1 % weight loss (P = 0.024).
Conclusion
A short-term mild-to-moderate weight loss in overweight normoglycemic subjects effectively improved their beta-cell function.
{"title":"Effect of short-term (4 weeks) low-calorie diet induced weight loss on beta-cell function in overweight normoglycemic subjects: A quasi-experimental pre-post interventional study","authors":"Monica Peter , Mithra Balaji , Joe Varghese , Sam Marconi , Yesudhas Sudhakar , Felix Jebasingh , Padmanaban Venkatesan","doi":"10.1016/j.metop.2025.100378","DOIUrl":"10.1016/j.metop.2025.100378","url":null,"abstract":"<div><h3>Introduction</h3><div>Diabetes in South Asians is driven primarily by impaired beta-cell function. When challenged with a high-calorie diet, this can result in metabolically unfavourable fat accumulation, which in turn worsens beta-cell function, thus constituting a vicious cycle. The investigators hypothesized that short-term mild-to-moderate weight loss induced by calorie restriction could break the cycle, resulting in significant improvements in beta-cell function. The objective of this study, therefore, was to evaluate the efficacy of a short-term weight loss program on body composition and beta-cell function.</div></div><div><h3>Methods</h3><div>As part of this quasi-experimental pre-post intervention study, 23 overweight normoglycemic participants underwent a low-calorie dietary intervention (∼1500 kcal/day) for a period of 4 weeks. Beta-cell function and insulin sensitivity were measured with a mixed meal challenge test (oral minimal model of glucose) before and after the intervention period. Changes in anthropometric parameters and body composition were also measured. The study was registered prospectively with the Clinical Trials Registry of India - CTRI/2023/04/051807 (<span><span>https://ctri.nic.in/</span><svg><path></path></svg></span>)</div></div><div><h3>Results</h3><div>Among the 23 participants in the study, 21 adhered to the intervention. The average weight loss was 3.5 % with an 11 % reduction in trunk fat mass. Beta-cell function, as measured by disposition index, increased by 128 % on average. Robust linear regression analysis showed that beta-cell function improved by 23 % for 1 % weight loss (P = 0.024).</div></div><div><h3>Conclusion</h3><div>A short-term mild-to-moderate weight loss in overweight normoglycemic subjects effectively improved their beta-cell function.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100378"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144524206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-24DOI: 10.1016/j.metop.2025.100373
Eleni C. Pardali , Christos Cholevas , Odysseas Androutsos , Christina Tsigalou , Dimitrios Poulimeneas , Dimitrios P. Bogdanos , Maria Dalamaga , Dimitrios G. Goulis , Maria G. Grammatikopoulou
Obesity is characterized by the expansion of adipose tissue, contributing to systemic low-grade inflammation, insulin resistance, and widespread disruption of metabolic pathways. These pathophysiological changes are strongly linked to the development of several chronic conditions, including metabolic syndrome, type 2 diabetes, cardiovascular disease, and certain forms of cancer. Metabolomics have emerged as a powerful analytical approach for elucidating obesity-related metabolic disturbances at both the cellular and systemic levels, enabling the identification of specific metabolic signatures associated with disease risk and progression.
This narrative review synthesizes findings from interventional weight loss studies that addressed obesity using various strategies, including dietary modification, physical activity, pharmacotherapy, and bariatric surgery. Focusing on studies employing metabolomic techniques, this review highlights both consistent and divergent patterns in metabolite changes observed following weight loss, particularly in the metabolism of amino acids, lipids, short-chain fatty acids, and other metabolic pathways affected by each intervention. These insights have the potential to inform the development of more personalized and effective therapeutic approaches for obesity, thereby advancing the implementation of precision medicine in obesity management.
{"title":"Interventional approaches to combat obesity: Exploring the metabolomic signature of weight loss trials","authors":"Eleni C. Pardali , Christos Cholevas , Odysseas Androutsos , Christina Tsigalou , Dimitrios Poulimeneas , Dimitrios P. Bogdanos , Maria Dalamaga , Dimitrios G. Goulis , Maria G. Grammatikopoulou","doi":"10.1016/j.metop.2025.100373","DOIUrl":"10.1016/j.metop.2025.100373","url":null,"abstract":"<div><div>Obesity is characterized by the expansion of adipose tissue, contributing to systemic low-grade inflammation, insulin resistance, and widespread disruption of metabolic pathways. These pathophysiological changes are strongly linked to the development of several chronic conditions, including metabolic syndrome, type 2 diabetes, cardiovascular disease, and certain forms of cancer. Metabolomics have emerged as a powerful analytical approach for elucidating obesity-related metabolic disturbances at both the cellular and systemic levels, enabling the identification of specific metabolic signatures associated with disease risk and progression.</div><div>This narrative review synthesizes findings from interventional weight loss studies that addressed obesity using various strategies, including dietary modification, physical activity, pharmacotherapy, and bariatric surgery. Focusing on studies employing metabolomic techniques, this review highlights both consistent and divergent patterns in metabolite changes observed following weight loss, particularly in the metabolism of amino acids, lipids, short-chain fatty acids, and other metabolic pathways affected by each intervention. These insights have the potential to inform the development of more personalized and effective therapeutic approaches for obesity, thereby advancing the implementation of precision medicine in obesity management.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100373"},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144489992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-23DOI: 10.1016/j.metop.2025.100377
Yuriko Hajika, Yuji Kawaguchi
For optimal postprandial glucose (PPG) management, rapid-acting insulin analogs (RAA) should be administered 15 min before a meal; however, this may not be possible for some individuals. Ultra-rapid lispro (URLi) can be administered 0–2 min before or <20 min after a meal, which may improve patient satisfaction and PPG management. In this pilot study, we evaluated changes in quality of life (QOL) and glycemic management among Japanese outpatients with type 2 diabetes mellitus (T2DM) who switched from RAA to URLi. We enrolled 12 outpatients with T2DM and evaluated QOL using the insulin therapy-related (ITR) QOL questionnaire. The primary endpoint was the change in ITR-QOL scores at 12–15 weeks. Endpoints were evaluated using the one-sample Wilcoxon signed rank test or paired t-tests. URLi was associated with a significant increase in ITR-QOL (+15.1 ± 16.1 points, p < 0.01), perception (+7.2 ± 6.9 points, p < 0.01), and status (+7.9 ± 9.5 points, p < 0.05) scores. At 12–15 weeks, the time in range significantly increased (+8.3 ± 9.2, p < 0.05), time above range significantly decreased (−7.7 ± 10.2, p < 0.05), and time below range showed no significant changes. Thus, switching from RAA to URLi significantly improved ITR-QOL questionnaire scores. In summary, URLi is an effective treatment alternative, providing flexible timing, improved glycemic management, and enhanced patient satisfaction.
{"title":"Improved quality of life and glycemic management after switching from conventional rapid-acting insulin to ultra-rapid lispro in patients with diabetes","authors":"Yuriko Hajika, Yuji Kawaguchi","doi":"10.1016/j.metop.2025.100377","DOIUrl":"10.1016/j.metop.2025.100377","url":null,"abstract":"<div><div>For optimal postprandial glucose (PPG) management, rapid-acting insulin analogs (RAA) should be administered 15 min before a meal; however, this may not be possible for some individuals. Ultra-rapid lispro (URLi) can be administered 0–2 min before or <20 min after a meal, which may improve patient satisfaction and PPG management. In this pilot study, we evaluated changes in quality of life (QOL) and glycemic management among Japanese outpatients with type 2 diabetes mellitus (T2DM) who switched from RAA to URLi. We enrolled 12 outpatients with T2DM and evaluated QOL using the insulin therapy-related (ITR) QOL questionnaire. The primary endpoint was the change in ITR-QOL scores at 12–15 weeks. Endpoints were evaluated using the one-sample Wilcoxon signed rank test or paired <em>t</em>-tests. URLi was associated with a significant increase in ITR-QOL (+15.1 ± 16.1 points, <em>p</em> < 0.01), perception (+7.2 ± 6.9 points, <em>p</em> < 0.01), and status (+7.9 ± 9.5 points, <em>p</em> < 0.05) scores. At 12–15 weeks, the time in range significantly increased (+8.3 ± 9.2, <em>p</em> < 0.05), time above range significantly decreased (−7.7 ± 10.2, <em>p</em> < 0.05), and time below range showed no significant changes. Thus, switching from RAA to URLi significantly improved ITR-QOL questionnaire scores. In summary, URLi is an effective treatment alternative, providing flexible timing, improved glycemic management, and enhanced patient satisfaction.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"27 ","pages":"Article 100377"},"PeriodicalIF":0.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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